Week 9 Flashcards
What are the main orders and genera of protozoa?
What are the common “groupings” of protozoa?
Generally what are protozoa? How many are parasitic? Locomotion? Nutrition?
What are the four main ways of locomotion for protozoa?
Avian trichomoniosis
Leishmaniosis
Cattle- neosporosis
What is a apicocomplexa?
Apicomplexa- to penetrate host cells
What is the apical complex of protozoa?
Apical complex- assists invasion of host cell… once inside–> forms Parasitophorus Vacuole- asexual multiplication by binary fision inside
Canine babesiosis
what is sporulation?
Unless they are sporulated (= embryonated) they are not infective
Within the oocyst.
What is the apicomplexan life cycle (direct)?
* once sporulated and in the cell–> merogany (each species have a certain number of cycles of merogany- the faster and the more cycles the more pathogenic the organism is)–> cell will rupture= causes necrosis–> once the zoites start multiplying they are known as merozoites–> rupture the cell–> repenetrate–> can become macrogametes (female form) or microgametes (male form)–> matures to form an oocyst (which exits the faeces UNSPORULATED- takes 3 days– sporulate and become infective)
What is schizogony? What is the starting age and product?
What is gametogony? Starting age? And product?
What is sporogony? Starting age? And product?
How do you generally identify sporulated oocyst?
** error Sarcocystis– 0:2:4 (sporocysts in faeces)
Cryptosporidium 1:0:4
Divisions of faecal transmitted eucoccidia?
If you see unsporulated oocysts in faeces, what is it likely to be?
coccidia
Eimeria and Cystisospora- Definitive host? Effect on host? Husbandry risk factors?
* species specificity has to do with immunity of species
Unsporulated and sporulated oocysts of Cystisospora
Eimeria and Cystisospora
Predisposing risk factors coccidiosis in livestock?
** usually younger susceptible animals
* overcrowding, changes in feed, etc.
Vector-borne apicomplexa
Eimeria- DH? Significance? Pathogenecity?
Eimeria Life Cycle
Eimeria
How do Ionophore Antibiotics work?
Kill Merozoites once they exit the cell- used to prevent- not curative
Ionophores are coccidiostatic- prevent it from getting worse
What’s good about this? You don’t want to kill all of them, you want to limit clinical infection and get the host to mount an immune response so that it is protected for the rest of its life
** would have to give continuously in water for example to use as a “cidal” agent
What is toltrazuril?
If you want to cure infection- give repeat doses- which we do when we are dealing with dogs and cats with diarrhoea
* Kills the intracellular forms of zoites as well– will kill mirozoites, macrogametes, developing zygote
Sulfonamides
* used mostly in mammals or small animals
Treatment and control of Eimeria
* not allowed to give layers cocciostatic or cidal drugs
Name Eimeria: 4 most pathogenic in poultry? Dogs and cats? Rabbit?
Coccidial infection in chickens- site of infection tenella? other species?
* only faecal flotation in pet chook
Key symptoms of E. tenella?
Bloody droppings, marked drop in feed consumption, emaciation, high rate of mortality, lethargy is very noticeable
Coccidiosis control in poultry
* bleach on concrete with oocysts will encourage sporulation- you must use an ammonia compound. There are special ones just for coccidia that are industrial strength used in these type of facilities. Desiccation will also do it.
** it can live in the environment for months- sometimes up to a year
** “too clean” is also a problem– if flock is completely naive to coccidiosis- high mortalities if there is an introduction
* want to vaccinate against the 4 most pathogenic ones– coccidiostats in feed or water
Feline tritichomoniosis
Congenital toxoplasmosis
Porcine coccidiosis
the nodules are filled with milky fluid that are protozoa
At risk of what?
Treat the ewe with coccidiostat in feed in late gestation
Coccidiosis
what are the three groupings in Apicomplexa?
Life cycle of Isospora (aka Cystoisospora)
* in some of the species: can use paratenic hosts in the life cycle if they ingest a sporulated oocyst- instead of the intestinal cycle occuring- the zooites enter the blood stream–> extra intestinal tissue (mostly muscle)–> form bradyzoites– slowly forming zoites
Risk: poor hygiene, stress
Clinical: in young
** acquired immunity- adults will still shed but not clinically affected, but a source for puppies and kittens
** never bloody- if it is bloody, something else going on (bacterial, or another parasite- hookworm)
Treatment and control of Cystisospora– diagnosis?
Diagnosis: faecal float- do not need to sporulate, as you just treat
necropsy- Dilated intestines
histo- Early stages of mirogamy
* no blood in faeces, just scours
* environment is filthy
* confined system
When did it start? Have coccidiostats been given? DDx? Cryptosporidium, Rotovirus, E. coli (colibacilliosis), Perfringens, Strongyloides ransomi (scours in neonatal piglets)
* take faecal sample– sporulate them over a few days– will have Eimeria spp. but non-pathogenic– but looking to see Isospora
Control options piglets Coccidiosis
* ammonia based cleaner
* oral coccidiostats at 3-5 days of age
* treat sows in feed with coccidiostat
What is the only non- host specific C. parvum? Name main species
Where do Cryptosporidium hang out?
* tiny sitting just under the membrane- extracystoplasmic- intracellular– called “epicellular”
* poultry- one species in respiratory epithelium
Differences:
* immediately infective
* they have normal oocysts “thick walled” but also “thin walled” oocysts– that can reinfect the same host– the reason it is a killer in an immuno compromised host
Pathogenesis of Cryptosporidium
Significance of Cryptosporidium
* resistant to normal levels of chlorine in the pool
* no drug to treat Cryptosporidium
what are the species of Cryptosporidium that infect humans?
(species infecting birds, cats, and dogs- immunocompromised humans susceptible)
What is the main problem with C. parvum?
Low infectious dose
Diagnosis of Cryptosporidium
Treatment of Cryptosporidium
Control of Cryptosporidium
Life cycle of Toxoplasma gondii
extraintestinal= multiplying in tissues
tachyzoites= multiplying rapidly; bradyzoites= slowed down
*vertical can maintain only the tissue stages (cat to her kitten) (transplacental spread)
** LOW host specificity– range of warm blooded mammals, including humans
* life long immunity once you’ve had it
Transmisson of Toxoplasma gondii
Immunity of Toxoplasma gondii
Can be infected, but not shed (in the tissues)- rarely after their first infection will a cat shed it in faeces (antibodie levels stay constantly high life long)
premunition = life long immunity in all hosts (e.g. can’t become tachyzoites because the antibodies are keeping them in check)
** problem is immunocompromised– they are able to multiply rapidly and destroy tissue- brain, placenta, fetus, lungs, ocular– “multi systemic disease”
Pathogenesis of Toxoplasma gondii
Significance of Toxoplasma gondii
Clinical signs of Toxoplasmosis
Toxoplasmosis in dogs
* not seen in a healthy dog
* damage depends on where the tachyzoites are multiplying
Public Health Significance of Toxoplasma gondii
When could a pregnant woman vertically transmit Toxoplasma gondii?
HIV/AIDs, infection contracted vertically potentially
What are the consequences of vertical transmission of Toxoplasma gondii in humans?
Diagnosis of T. gondii
More likely extra-intestinal. Cat with clinical seizures. What sample would you take? CSF. Pneumonia? IgM, IgG titre. PCR– you have to go for the tissue itself.
* Even if you acquire a kitten shedding oocysts in the faeces- would not get infected because they haven’t sporulated yet– could happen but chances are low even if cat has FIV
Treatment of T. gondii
Prevention and control of T. gondii
Life cycle of Neospora caninum, is it a zoonosis? Most common route of infection for dogs?
No.
* ingesting raw beef
* will never see clinically in an adult dog, only small dogs
* major cause of abortion in cattle
Significance of Neospora caninum
Clinical signs of Neospora caninum in dogs
Diagnosis, Treatment and Prognosis
* If from affecting litter- do not breed with bitch again
* source of infection either vertical from her Mom- or through ingestion of raw meat
* (Corticosteroids might make it worse, if unknown diagnosis, could potentially give)
Compare and contrast T. gondii and N. caninum?
Sarcocystis life cycle
* Many host-specific species (> 130)
* Canids/ felids/ humans DH- gametogony + sporogony
* Herb/omnivore IH- merogony- tissue cysts
* highly host specific
Significance of Sarcocystis
In Australia- No big deal to ingest- infective to dogs though!!
* other countries- can result in condemnation of meat
* young horses in the USA- predilection for the brain- Equine protozoal myeloencephalitis
Sarcocystosis in Humans
Diagnosis of Sarcocystis
* DH- sporocysts in faeces
* IH- histopathology, then PCR, bradyzoites
Treatment and control of Sarcocystis
Usually not required
* Don’t feed raw meat
